RODS ARE SELECTIVELY ALTERED BY LEAD .2. ULTRASTRUCTURE AND QUANTITATIVE HISTOLOGY
RODS ARE SELECTIVELY ALTERED BY LEAD .2. ULTRASTRUCTURE AND QUANTITATIVE HISTOLOGY
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DOI：
10.1016/s0014-4835(88)80017-4
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发表时间：
1988-04-01
影响因子：
3.4
通讯作者：
CHU, LWF
中科院分区：
文献类型：
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作者：
FOX, DA;CHU, LWF
视网膜电图和环核苷酸代谢的研究已经确定，低水平的铅暴露在出生后早期的发展结果在长期的选择性杆缺陷。为了确定是否有相应的选择性视杆细胞变性，我们研究了成年大鼠视网膜暴露于低水平的铅在发展过程中使用光学和电子显微镜。在所有的视网膜区域中，观察到杆细胞而不是锥细胞变性。总的来说，20%的视杆细胞丢失。此外，还发现了两个特殊的区域差异：下视网膜变性（-25%）远大于上级（-15%），后视网膜变性（-22%）远大于周边（-17%）。后一种模式表明中央-外周梯度变性。总视网膜厚度减少15- 20%，这反映了外核层和内核层中的细胞损失。在超微结构上，铅诱导的最明显的改变是杆外节肿胀和紊乱，以及杆感光细胞线粒体中大量β-糖原颗粒的积聚。糖原积累最重的杆内段线粒体，其次是杆轴突和突触末端线粒体。导致这些铅诱导的视网膜改变的可能的细胞作用机制包括抑制视网膜环GMP磷酸二酯酶和由此产生的环GMP升高、抑制中间代谢和/或改变钙代谢。此外，内核层变薄可能是由于跨神经元变性。正如我们在前面的论文中所指出的，第一种可能性已经在类似暴露于铅的大鼠中得到了证明。这些定量的组织学结果，结合ERG和生化结果在前面的文件中，表明，低水平的铅暴露在出生后的早期发展产生长期的选择性和功能缺陷和退化。
Electroretinographic and cyclic nucleotide metabolism studies have established that low-level lead exposure during early postnatal development results in long-term selective rod deficits. To determine whether there was a corresponding selective rod photoreceptor cell degeneration we examined retinas of adult rats exposed to low-level lead during development using light and electron microscopy. In all retinal regions, a rod but not cone cell degeneration was observed. Overall, 20% of the rod cells were lost. Moreover, two specific regional differences were found. Degeneration was much greater in the inferior (-25%) than superior (-15%) retina and greater in the posterior (-22%) than peripheral (-17%) retina. The latter pattern indicates a central-peripheral gradient of degeneration. Total retinal thickness decreased 15-20%, which reflects cell loss in the outer and inner nuclear layers. Ultrastructurally, the most obvious lead-induced alterations were swollen and disorganized rod outer segments and large accumulations of beta-glycogen particles in rod photoreceptor mitochondria. Glycogen accumulations were heaviest in rod inner segment mitochondria followed by rod axon and synaptic terminal mitochondria. Possible cellular mechanisms of action responsible for these lead-induced retinal alterations include an inhibition of retinal cyclic GMP phosphodiesterase and the resultant elevation of cyclic GMP, an inhibition of intermediary metabolism and/or an alteration in calcium metabolism. In addition, the thinning of the inner nuclear layers could be due to transneuronal degeneration. As noted in our preceding paper, the first possibility has been demonstrated in rats similary exposed to lead. These quantitative histological results, in combination with the ERG and biochemical results in the preceding paper, demonstrate that low-level lead exposure during early postnatal development produces long-term selective and functional deficits and degeneration.